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Extension Toxicology Network

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.


Publication Date: 9/95


The active ingredient dicrotophos is found in a variety of commercial insecticides. Trade names for products containing dicrotophos include Bidrin, Carbicron, Diapadrin, Dicron and Ektafos (4, 8, 19).


Dicrotophos is a Restricted Use Pesticide (RUP). Restricted use pesticides may be purchased and used only by certified applicators. Check with specific state regulations for local restrictions which may apply. Products containing dicrotophos must bear the Signal Word "Warning" on their label (4).


Dicrotophos was introduced in 1956 as a contact systemic pesticide with a wide range of applications. The E-isomer is more insecticidally active than the Z-isomer. Dicrotophos is available as 24% and 85% concentrates, as 40% and 50% emulsifiable concentrates, water-soluble concentrates and ULV formulations (1, 2, 4, 7, 14, 16). Dicrotophos is classified as a systemic insecticide and acaricide of moderate persistence. It is effective against sucking, boring and chewing pests, and is recommended for use on coffee, cotton, rice, pecans and other crops. In animal health, it is used for control of ticks and lice on cattle at a concentration of 50 grams ai/100 liters (12). Dicrotophos is non-phytotoxic except to certain varieties of fruit under some conditions (2, 5). The material enters plant tissue rapidly, which enables many beneficial insects to survive (4).

Dicrotophos has been used on elm trees in an attempt to control Dutch elm disease (which is spread by a beetle), as well as to control pests on cotton and soybeans (18).



Dicrotophos is a compound of rather high oral and dermal toxicity (14). The acute oral LD50 for rats ranged from 13-25 mg/kg (2, 4, 5, 6, 19); and ranged from 11-15 mg/kg for mice (1, 6). Another source reported the subcutaneous LD50 for rats to be 8137 micrograms/kg, and 11,500 micrograms/kg for the mouse. The intravenous LD50 for the mouse is 9,900 micrograms/kg; and the intraperitoneal LD50 is 9,500 micrograms/kg (6).

The reported acute percutaneous LD50 for rats ranges from 111-136 mg/kg to 148-181 mg/kg, depending on the carrier and the conditions of the test. The dermal LD50 for the rat was 42 mg/kg. The dermal LD50 values for rabbits ranged from 168 mg/kg to 225 mg/kg (1, 2, 4, 6); dicrotophos caused slight irritation to the skin and eyes of rabbits (2).

The 4-hour inhalation LC50 value for rats exposed to dicrotophos was 90 mg/m3 air (2, 6). The inhalation LC50 for rats exposed to aerosol was 0.61- 0.91 mg/l/hour (1).

Dicrotophos emits toxic fumes of phosphorus and nitrogen oxides when heated to decomposition (11). In two human poisoning cases, symptoms such as cramps, nausea, vomiting, diarrhea, dyspnea, and general weakness occurred when exposed to spray, and loss of pulse and respiration occurred when ingested. In both cases, atropine and pralidoxime relieved the symptoms and the patients showed improvement. However, in both cases, the patients relapsed within 7 to 10 days. Both finally returned to normal at 22 and 23 days (14, 16).

The acute oral LDlo for humans was reported to be 5 mg/kg (10). Symptoms of exposure include: headache, anorexia, nausea, vertigo, weakness, abdominal cramps, diarrhea, salivation, lacrimation, ataxia, cyanosis, pulmonary edema, convulsions, coma and shock (11).


In 2-year feeding trials, the no effect level (NEL) was 1.0 mg/kg diet (0.05 mg/kg daily) for rats; and 1.6 mg/kg diet (0.04 mg/kg daily) for dogs (2). Dicrotophos fed to rats at 15-45 mg/kg body weight for 90 days had no adverse effect on growth or any of the more pronounced pathological changes observed when dicrotophos was fed at 135 mg/kg (1).

In 2-year feeding studies, the threshold for cholinesterase depression was 10 ppm in rats and 16 ppm in dogs. Dicrotophos is considered a cholinesterase inhibitor (6).

Reproductive Effects

The NEL in a three-generation reproduction study with rats was determined to be 2 mg/kg daily (2). Studies where intraperitoneal injections of dicrotophos were given to pregnant mice caused no morphological anomaly. No changes in the developmental patterns of brain acetylcholinesterase or choline acetyltransferase were seen, even though embryonic or fetal acetylcholinesterase levels were reduced (16).

In two reproductive studies in rats, no reproductive effects were noted at 2 and 3 ppm in diet. At higher levels, reproductive and fetotoxic effects were noted (3). Dicrotophos may cross the placenta (6).

Another study reported that dicrotophos at 50 ppm in the diet of pregnant rats caused an increase in the number of embryos absorbed (9.7% versus 1.14% in controls) at the 17th day of pregnancy. At 100 ppm there was a 26.5% reduction of conceptuses. No gross abnormalities were observed in the surviving fetuses and no maternal toxicity was observed (19).

Teratogenic Effects

There were no teratogenic responses noted in laboratory animals (3). Dicrotophos has a teratogenic effect in birds at dosages of 0.1 mg/egg (16).

Mutagenic Effects

Technical Bidrin (a product containing dicrotophos) exhibited low mutagenic potential (3). Dicrotophos is a suspect mutagen to mammals (8).

Carcinogenic Effects

No carcinogenic effects were noted (6).

Organ Toxicity

Increases in kidney, spleen, liver and testes weights occurred in male rats and increases in kidney weights were noted in female rats at 135 ppm. Some liver effects were noted at a dose 10 times that eliciting cholinesterase depression (3).

Fate in Humans and Animals

Dicrotophos is metabolized in part to monocrotophos. The concentration of monocrotophos in tissues may be higher than that of the parent compound in a few hours after administration. Residues of both compounds are dissipated almost entirely within 24 hours (16). The most significant effect noted was reversible cholinesterase depression at thresholds of 1.5 and 5 ppm in rats and dogs, respectively (3).

The most predominant detoxicating reaction is hydrolysis of the vinyl- phosphate bond of dicrotophos or its oxidative metabolites to produce dimethyl phosphate. The proportion of dimethyl phosphate in the urine of rats increases rapidly after dosing, reaching 50% of all metabolites present in less than 4 hours and over 80% in 20 hours. Dicrotophos is rapidly excreted in rats. After 6 hours, 65% of the injected dose was excreted, and after 24 hours, 83% was excreted in urine alone (16).

Milk and feces from cows maintained for 28 days on 15 ppm dicrotophos (approximately 0.23 mg/kg body weight) contained no detectable (less than 0.002 ppm for milk, less than 0.004 ppm for feces) dicrotophos or monocrotophos. Urine contained 2 to 5% of the ingested dose as monocrotophos and dicrotophos (70% and 30%, respectively, of the material recovered from the urine) (19).

Dicrotophos oxidized to des-N-methyl derivatives by liver microsomal enzymes (17). The compound and its metabolites did not accumulate in tissue and no bioaccumulation occurs (19).


Effects on Birds

The acute oral LD50 for birds ranged from 1.2-12.5 mg/kg. Specifically, the LD50 for the pigeon is 2 mg/kg, 7,970 micrograms/kg for the chicken, 4 mg/kg for the quail and 4,140 micrograms/kg for the duck (9, 10). Immediate toxicity to birds is considered very high (8).

Dicrotophos is not neurotoxic to hens (2).

Effects on Aquatic Organisms

The 24-hour LC50 for mosquito fish was 200 mg/l; and greater than 1,000 mg/l for harlequin fish (1, 2). The immediate toxicity to fish is considered low to medium (LD50 greater than 5,000 mg/kg). The immediate toxicity to amphibians is medium (LD50 500-5,000 mg/kg); medium to high (LD50 50-5,000 mg/kg) for crustaceans; and high (50-500 mg/kg) for aquatic insects (8).

Effects on Other Animals (Nontarget species)

Dicrotophos is considered very toxic to honeybees, but because surface residues rapidly decline, little effect is seen in actual practice (2). The relative toxicity of dicrotophos to the adult parasitoid Microplitis croceipes is high (13).

Birds and wildlife in treated areas may be killed (5).


Breakdown of Chemical in Soil and Groundwater

Hydrolysis rates of dicrotophos in the aqueous and soil environment are pH-dependent and follow first-order kinetics. The half-lives of dicrotophos in pH 5, 7, and 9 buffer solutions are 117, 72, and 28 days, respectively. N,N-Dimethylacetoacetamide and O-desmethyldicrotophos are the major hydrolytic degradation products. Dicrotophos degradation is not induced by exposure to light. Dicrotophos has intermediate soil mobility. Dicrotophos and its degradation products do not persist in the environment (15).

In soil, the dimethylamino group is converted to an N-oxide then to CH2OH and aldehyde groups, which further degrade via demethylation and hydrolysis. Dicrotophos is rapidly degraded under both aerobic and anaerobic conditions forming N,N-dimethylbutyramide as the major metabolite. Other metabolites include carbon dioxide and unextractable residues. The half-life of dicrotophos in a Hanford sandy loam soil was three days (11).

Breakdown of Chemical in Surface Water

No information was available.

Breakdown of Chemical in Vegetation

Dicrotophos is considered nonphytotoxic when used at the recommended rates. It may be harmful to some varieties of grain seed. More than 50% of the material is absorbed into the plant within 8 hours of application (5). It may be phytotoxic to certain varieties of fruit under some conditions (9).


Exposure Guidelines:

TLV-TWA: 0.25 mg/m3 (11)
PEL: 0.25 mg/m3 (11)

Physical Properties:

The technical material consists of 85% E-isomer (16). Dicrotophos is stable when stored in glass or polythene containers up to 40 degrees C, but is decomposed after 31 days at 75 degrees C or 7 days at 90 degrees C. The half- life of an aqueous solution at 38 degrees C and a pH of 9.1 is 50 days, and at a pH of 1.1 the half-life is 100 days. It is corrosive to cast iron, mild steel, brass and some grades of stainless steel (9, 19).

Appearance: the pure material forms a yellow to brown liquid with a mild ester-like odor (11)
CAS No.: 141-66-2 (1, 6) 3725-78-2 for the mined isomers, 141-66-2 for the E-isomer and 18250-63-0 for the Z-isomer (16)
Molecular formula: C8H16NO5P (16)
Molecular weight: 237.21
Chemical name: dimethyl (E)-2-dimethylcarbamoyl-1-methylvinyl phosphate (1, 4); 3-dimethoxyphosphinyloxy-N, N-dimethylisocrotonamide. E-isomer of O,O-dimethyl-O-(3-dimethylamino-1-methyl-3-oxo-1-propenyl) phosphate (16)
Chemical Class/Use: organophosphate/contact, systemic insecticide (4)
Specific gravity: technical 1.216 at 20 degrees C (6, 11) pure 1.468 at 23 degrees C (9)
Solubility in water: Miscible with water
Solubility in other solvents: Miscible with acetone, alcohol, acetonitrile, chloroform, methylene chloride, and xylene. Barely soluble in mineral oils (1). Slightly soluble in kerosene and diesel fuel (<1%) (6, 12)
Melting point: <25 degrees C (11)
Boiling point: 266 degrees F (130 degrees C) @ 0.1 mmHg (2, 6); 90-95 degrees C at 0.0013 mbar (1); technical, 400 degrees C (16)
Decomposition temperature: at 38 degrees C, 50% decomposition occurs in 1200 hours at pH 9.1; 50% decomposition occurs in 2400 hours at pH 1.1 (1)
Flashpoint: >200 degrees F (4)
Vapor pressure: 9.3 mPa at 20 degrees C (2); technical, 1 x 10 to the minus 4 mmHg at 20 degrees C (16, 19); Pure, 6.98 x 10 to the minus 5 mmHg at 20 degrees C (11)
log Koc: 1.04 - 2.27 (11)
log Kow: 0.50 (11)


AMVAC Chemical Corporation
4100 E. Washington Blvd.
Los Angeles, CA 90023
Telephone: 213-264-3910
Fax: 213-268-1028

Review by Basic Manufacturer:

Comments solicited: October, 1994
Comments received:

P.O. Box 18300
Greensboro, NC 27419-8300
Telephone: 919-632-6000
Emergency: 800-334-9481 Ext. 7745

Review by Basic Manufacturer:

Comments solicited: October, 1994
Comments received:


  1. The Agrochemicals Handbook. 1983. The Royal Society of Chemistry, The University, Nottingham, England.
  2. Worthing, C. R. (ed.). 1983. The Pesticide Manual: A World Compendium. Seventh edition. Published by The British Crop Protection Council.
  3. MSDS for Technical Bidrin. 1985. Shell Oil Company, Product Safety and Compliance. Houston, TX.
  4. Farm Chemicals Handbook. 1993. Meister Publishing Co. Willoughby, OH.
  5. Thomson, W. T. 1989. Agricultural Chemicals. Book I: Insecticides. Thomson Publications, Fresno, CA.
  6. OHS Database. 1993. Occupational Health Services, Inc. 1993 (August) MSDS for Dicrotophos. OHS Inc., Secaucus, NJ.
  7. Thomson, W. T. 1992. Agricultural Chemicals Book I: Insecticides. Thomson Publications, Fresno, CA.
  8. Briggs, S. A. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards. Hemisphere Publishing Corp., Washington, Philadelphia, London.
  9. Worthing, C. R. (ed.). 1987. The Pesticide Manual: A World Compendium. Eighth edition. Published by The British Crop Protection Council.
  10. Fairchild, E. J. (ed.). 1977. Agricultural Chemicals and Pesticides: A Subfile of the Registry of Toxic Effects of Chemical Substances. U. S. Department of Health, Education, and Welfare, Cincinatti, OH.
  11. Montgomery, J.H. (ed.). 1993. Agrochemicals Desk Reference. Environmental Data. Published by Lewis Publishers, Chelsea, MI.
  12. Spencer, E. Y. 1981. Guide to the Chemicals Used in Crop Protection. 7th edition. Publication 1093. Research Branch. Agriculture Canada.
  13. Elzen, G. W. 1989. Sublethal Effects of Pesticides on Beneficial Parasitoids. In: Pesticides and Non-target Invertebrates. Ed. by Paul C. Jepson. Intercept Ltd. Dorset, England. pp 129-150.
  14. Hayes, W.J., Jr. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Classes of Pesticides, Vol. 2. Academic Press, Inc., NY.
  15. Lee, P. W., S. M. Stearns, Hector Hernandez, W. R. Powell and M. V. Naidu. 1989. Fate of Dicrotophos in Soil. J. Agric. Food Chem. 37:1169-11174.
  16. Hayes, W. J., Jr. 1982. Pesticides Studied in Man. Williams and Wilkins. Baltimore, London.
  17. Hayes, W.J., Jr. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, General Principles, Vol. 1. Academic Press, Inc., NY.
  18. Hassall, K. A. 1990. The biochemistry and Uses of Pesticides: Structure, Metabolism, Mode of Action and Uses in Crop Protection. 2nd Edition. VCH Publishers, NY.
  19. U.S. Environmental Protection Agency. April, 1982. Guidance for the Reregistration of Pesticide Products Containing Dicrotophos as the Active Ingredient. US EPA, Office of Pesticide Programs, Registration Div., Washington, DC.